Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells

Mark H. Kaplan, Ulrike Schindler, Stephen T. Smiley, Michael J. Grusby

Research output: Contribution to journalArticle

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Abstract

Interleukin-4 (IL-4) stimulation of cells leads to the activation of multiple signaling pathways, one of which involves Stat6. We have generated Stat6-deficient mice by gene targeting in embryonic stem cells to determine the role of this transcription factor in mediating the biologic functions of IL-4. IL-4-induced increases in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrogated, and lymphocytes from Stat6-deficient animals fail to proliferate in response to IL-4. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. In addition, Stat6-deficient T lymphocytes fail to differentiate into Th2 cells in response to either IL-4 or IL-13. These results demonstrate that, despite the existence of multiple signaling pathways activated by IL-4, Stat6 is essential for mediating responses to IL-4 in lymphocytes.

Original languageEnglish (US)
Pages (from-to)313-319
Number of pages7
JournalImmunity
Volume4
Issue number3
DOIs
StatePublished - Mar 1996

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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